November 1998
Volume 39, Issue 12
Free
Articles  |   November 1998
Retinal vasculature changes in Norrie disease mice.
Author Affiliations
  • M Richter
    Department of Anatomy II, University of Erlangen-Nürnberg, Erlangen, Germany.
  • J Gottanka
    Department of Anatomy II, University of Erlangen-Nürnberg, Erlangen, Germany.
  • C A May
    Department of Anatomy II, University of Erlangen-Nürnberg, Erlangen, Germany.
  • U Welge-Lüssen
    Department of Anatomy II, University of Erlangen-Nürnberg, Erlangen, Germany.
  • W Berger
    Department of Anatomy II, University of Erlangen-Nürnberg, Erlangen, Germany.
  • E Lütjen-Drecoll
    Department of Anatomy II, University of Erlangen-Nürnberg, Erlangen, Germany.
Investigative Ophthalmology & Visual Science November 1998, Vol.39, 2450-2457. doi:
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    • Get Citation

      M Richter, J Gottanka, C A May, U Welge-Lüssen, W Berger, E Lütjen-Drecoll; Retinal vasculature changes in Norrie disease mice.. Invest. Ophthalmol. Vis. Sci. 1998;39(12):2450-2457.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: To correlate morphologic changes in the retinal vasculature with degenerative changes in the neuronal retina of mice lacking 56 amino acids from the N-terminus of the Norrie disease (ND) gene product. METHODS: Posterior eye segments of ND mice of different age groups were investigated by light and electron microscopy (EM) and scanning EM of vascular corrosion cast preparations. The results were qualitatively and quantitatively compared with those obtained in age-matched littermate control mice and C57B1/6 mice. RESULTS: Quantitative evaluation revealed an increase in the number of blood vessels in the interface of the ganglion cell layer and the nerve fiber layer and a decrease in the inner and outer plexiform layers in ND mice older than 9 days compared with control mice. Vessels were also seen adjacent to the vitreous surface of the inner limiting membrane. Most of these vessels showed fenestrations and occasionally penetrated the inner limiting membrane. Hyaloid vessels were still present in the vitreous. The abnormal vascularization pattern was found in the entire retina and occurred in addition to the previously described alterations of the neuronal retina. CONCLUSIONS: There is a malformation of the retinal vasculature and a persistence of hyaloid vessels in the vitreous of ND mice. It is assumed that the ND gene product is required for normal vascularization of the inner retinal layers and for atrophy of hyaloid vessels.

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